The neutrophil is an important cell in the pathogenesis of periodontal disease as is indicated by an increase in disease in conditions where neutrophil function is impaired. Periodontosis, (Localized Juvenile Periodontitis, LJP) patients provide a model for compromised neutrophil function since reduction in chemotaxis has been identified in this group of patients which is consistent in character among subjects. The purpose of this study is to begin characterization of the biochemical basis for the reduction in chemotaxis of neutrophils from patients with LJP. Using a rapid filtration assay, the reduction of specific binding of radiolabelled chemotactic peptide will be characterized. In equilibrium and kinetic experiments, the differences in binding affinity and number of receptors available on the cell surface between LJP and control groups will be evaluated. To assess the presence of cryptic or blocked receptors, the surface topgraphy, spacial relationship and fate of protein and glycoprotein surface components, including the peptide receptor, will be examined. This will be accomplished using techniques employing surface labeling, bifunctional crosslinking reagents and affinity labeling of the receptor, before and after exposure of the neutrophil to chemotactic peptide. Additionally, experiments will be performed which are aimed at exposure to cryptic receptors using aliphatic alcohols. The fate of the chemotactic ligand after binding to LJP and control cells will be assessed by thin layer chromatography. Receptor regulation will be evaluated after assessment of ligand or receptor degradation, and blocking of the receptor. Extracts of bacteria isolated from periodontal lesions, known to inhibit neutrophil chemotaxis, will be evaluated for their effect upon binding of chemotactic peptides to the neutrophil. The extracts will be tested for protease activity, blocking of the peptide receptor on the neutrophil or down-regulation of the receptor. The long range goal of these studies is the furthering of our knowledge of the complex interactions of the neutrophil and its environment as it effects the inflammatory process and host defense.